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Murine Colitis Modeling using Dextran Sulfate Sodium DSS
Published on: January 19, 2010
[Paeoniflorin attenuates dextran sulfate sodium-induced ulcerative colitis in mice by inhibiting TLR5 expression and
Xiaojing Wang1, Xia Luo1, Zhongzheng Zhao2
1Department of Immunopharmacology, School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou 510006, China.
Abstract:
Objective To investigate the therapeutic effect and mechanism of paeoniflorin on dextran sulphate sodium (DSS)-induced ulcerative colitis (UC) mice. Methods C57BL/6 male mice were randomly divided into control group, model group, 600 mg/(kg.d) mesalazine treatment group, (12.5, 25, 50) mg/(kg.d) paeoniflorin treatment group, with 10 mice in each. All mice were treated with 30 g/L DSS for 5 days except the control group. Meanwhile, the mice in the other groups were orally administrated corresponding drugs for 10 days, while the mice in the control and model groups were given equivalent volumes of distilled water. Body mass, fecal characteristics and hematochezia of the mice were observed and recorded daily, and then disease activity index (DAI) was evaluated and calculated. Pathological changes in the colon were observed by HE staining. The levels of anti-flagellin antibody, interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) in the serum were measured by ELISA. The expression levels of Toll-like receptor 5 (TLR5), myeloid differentiation factor 88 (MyD88) and nuclear factor kappa-Bp65 (NF-κBp65) in the colon tissues were evaluated by Western blot analysis and the activation of lymphocytes in mesenteric lymph node (MLN) was detected by flow cytometry. Results Compared with the control group, DAI scores in the model group were significantly raised, the colon length was significantly shortened, and the epithelium and intestinal gland disappeared. In addition, the serum levels of anti-flagellin antibody, IL-6, TNF-α and the protein levels of TLR5, MyD88, NF-κBp65 in the colon significantly increased, and the activation of T lymphocytes in MLN went up in the model group. All symptoms above were alleviated in the mesalazine and paeoniflorin groups compared with the model group. Conclusion Paeoniflorin can attenuate UC in mice by inhibiting the expression of flagellin and TLR5, and the activation of T cells.
Insights
Paeoniflorin effectively treats ulcerative colitis (UC) in mice by reducing inflammation. It works by inhibiting flagellin and Toll-like receptor 5 (TLR5) expression and decreasing T cell activation, offering a potential therapeutic strategy for UC.
Area of Science:
- Pharmacology and Immunology
- Gastroenterology
Background:
- Ulcerative colitis (UC) is a chronic inflammatory bowel disease with complex pathogenesis.
- Dextran sulfate sodium (DSS)-induced colitis in mice serves as a standard model for studying UC.
- Paeoniflorin, a compound derived from Paeonia species, has shown anti-inflammatory properties.
Purpose of the Study:
- To investigate the therapeutic effects of paeoniflorin on DSS-induced ulcerative colitis in mice.
- To elucidate the underlying mechanism of paeoniflorin's action in this UC model.
Main Methods:
- Male C57BL/6 mice were induced with DSS to model ulcerative colitis.
- Mice were treated with varying doses of paeoniflorin or mesalazine (positive control).
- Disease activity index (DAI), colon histology, serum cytokine levels (IL-6, TNF-α), anti-flagellin antibody, and key protein expressions (TLR5, MyD88, NF-κBp65) were assessed.
Main Results:
- DSS-induced mice exhibited increased DAI, shortened colon, and significant inflammation.
- Paeoniflorin treatment significantly alleviated UC symptoms and pathological damage.
- Paeoniflorin reduced serum inflammatory markers and inhibited the expression of flagellin, TLR5, MyD88, and NF-κBp65, alongside decreased T cell activation.
Conclusions:
- Paeoniflorin demonstrates significant therapeutic effects in a mouse model of ulcerative colitis.
- The mechanism involves the inhibition of flagellin and Toll-like receptor 5 (TLR5) signaling pathway.
- Paeoniflorin also suppresses T lymphocyte activation, suggesting its potential as a novel treatment for UC.
